When one thinks of the motor system it is usually reduced to the direct corticospinal tract and the lower motor neuron (LMN). Although these 2 components are main stage players, it is important to add a few more components to our oversimplified scheme of the motor system.

Control Circuits

First, we need to add two "control circuits" that influence the corticospinal tract- the basal ganglia and the cerebellum.

Brainstem Motor Control Centers

There are also the indirect brainstem motor control centers and their pathways (rubrospinal, vestibulospinal, and reticulospinal) that tonically activate lower motor neurons, especially those that innervate axial and antigravity muscles (those motor neurons that are in the medial part of the ventral horn).

Upper Motor Neuron Lesion

The corticospinal tract has its main influence on the motor neurons that innervate the muscles of the distal extremities- the hand and the foot (motor neurons in the lateral part of the ventral horn). The corticospinal tract also (and this a key point) has collaterals that modulate and control the indirect brainstem motor centers so that we are not a stiff statue opposing gravity but rather we can move at will and have just the right amount of supporting tone. So when there is a lesion of the upper motor neuron (the UMN is the corticospinal tract and it's collaterals to the brainstem motor nuclei) the clinical findings are a combination of the loss of direct effect of the corticospinal tract on the LMN plus the loss of control and modulation of the indirect brainstem motor control centers.

UMN Lesion Clinical Findings

The clinical findings from a UMN lesion will include loss of distal extremity strength, dexterity and a Babinski sign (loss of direct corticospinal effect) plus increased tone, hyperreflexia, and the clasp-knife phenomenon (from loss of control of the indirect brainstem centers).

LMN Lesion Clinical Findings

Lesions of the LMN, "the final common pathway", result in loss of strength, tone and reflexes with the denervated muscle showing wasting and denervation hypersensitivity - fasciculations.

UMN Syndrome

Important point to remember:

  • The UMN syndrome is a combination of loss of the direct corticospinal tract effect on the LMN and the loss of regulation of the indirect brainstem motor control centers.

Decorticate vs. Decerebrate

  • A UMN lesion above the level of the red nucleus will result in decorticate posture(thumb tucked under flexed fingers in fisted position, pronation of forearm, flexion at elbow with the lower extremity in extension with foot inversion) while a lesion below the level of the red nucleus but above the level of the vestibulospinal and reticulospinal nuclei will result in decerebrate posture (upper extremity in pronation and extension and the lower extremity in extension). The reason for this is that the red nucleus output reinforces antigravity flexion of the upper extremity. When its output is eliminated then the unregulated reticulospinal and vestibulospinal tracts reinforce extension tone of both upper and lower extremities. If there is a lesion in the medulla then all the brainstem motor nuclei as well as the direct corticospinal tract would be out and the patient would be flaccid acutely. If the patient were to survive, tone would return because of interneuronal activity at the spinal cord level.

Localizing a UMN Lesion

  • An UMN lesion is on the opposite side of the clinical findings for a lesion above the decussation of the pyramids (where the corticospinal tracts cross) whereas it is on the same side as clinical findings if the lesion is in the spinal cord.

Spinal Cord Lesions

  • Spinal cord lesions often give UMN signs below the level of the lesion (from effect on the corticospinal tract) and LMN signs at the level of the lesion (from effect on the ventral horn or ventral nerve root).

  • LMN signs are good for locating the level of a spinal cord lesion.

Exam Tests

  • Clinical testing of the motor system:

  • Muscle strength

  • Tone 

  • Reflexes 

  • Pathological reflexes


  • Hypertonia can be either spasticity or rigidity. Spasticity is from a UMN lesion. It is rate dependent resistance on range of motion with collapse of the resistance at the end of the range of motion. This is called the clasp-knife phenomena. Rigidity is from basal ganglia disease. The resistance to range of motion is not rate or force dependent and is constant throughout the range of motion. This is often referred to as lead pipe or plastic-like rigidity.


  • Acute UMN lesions and UMN lesions in infants can produce hypotonia initially with hypertonia occurring later.

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